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Pericarditis - Diagnosis and Management Challenges
71
. Role of ANCA antibodies and neutrophils
ANCAs, which represent autoantibodies directed against neutrophil cytoplasmic proteins, recognize a range of antigens. Only two relevant protein targets are
identified, called proteinase 3 (PR3) and myeloperoxidase (MPO). These proteins
are found in the primary granules of neutrophils and are involved in defense against
microbes [5].
During AAV and in small vessels, a pathological and sustained interaction occurs
between ANCA and abnormally activated neutrophils. Thus, in the systemic form
of GPA, ANCAs recognize PR3 in about 75% of cases. Whereas MPO-ANCA is more
commonly associated with MPA (60%) and EGPA (50%) [5–7].
Experimental and clinical data provide evidence that ANCAs and neutrophils
are the key players in pathogenesis. In response to inflammation or infection,
neutrophils exposed to cytokines (interleukin 1, tumor necrosis factor α…) or
complement C5a become primed with movement of MPO and PR3 from primary
granules to the cell surface. ANCAs bind to these autoantigens on the neutrophil
surface. Neutrophils become activated and bind to vascular endothelium, resulting
in tissue damage.
. Role of the complement system, cellular and humeral immunity
The pathogenesis of AAV also involves [5–8]
A. Activation of the alternative complement pathway responsible for the amplifica-
tion of neutrophil-ANCA activation.
B. Monocytes and macrophages: in the formation of the classic GPA granuloma.
C. B and T lymphocytes: in the occurrence of endothelial damage and granuloma
formation.
D. Eosinophilic polynuclear cells: The blood level of eosinophils can be high in the
various vasculitis. These cells have cytotoxic granules that can contribute to
cardiac involvement and vascular damage as seen in EGPA [7].
. Predisposing factors for ANCA-associated vasculitis
A. Environmental factors:
• Pesticides, asbestos, smoke and silica.
• A number of therapeutic agents are responsible for drug-induced AAV such as
propylthiouracil, benzylthio-uracil and hydralazine … [5].
• Chronic carriage of staphylococcus aureus which is reported to be a risk factor
for relapse in GPA.
B. Genetic predisposition: Familial cases of AAV have been reported and predispos-
ing HLA haplotypes such as HLA DPB1 [8].
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. Classification and prognostic score of ANCA-associated vasculitis
72
. Classification criteria of ANCA-associated vasculitis:
.. Granulomatosis with polyangiitis
Granulomatosis with polyangiitis (GPA), formerly named Wegner’s disease, is
characterized by vessel wall inflammation, peri- and extra-vascular granulomatosis.
Its annual incidence is 10.2 cases per million people, and its prevalence is between 24
and 150 cases per million people [9]. Caucasians are the most affected persons according to researches conducted in Europe [10]. GPA is diagnosed at an age of 35–55years
with no gender predominance.
This disease involves mainly upper and lower airways, ear nose throat sphere
and kidney. Nasosinus involvement occurs in 70–100% of patients as epistaxis,
nasal septum deformation or perforation [11, 12]. Lungs manifestations affect
50–90% of the patients as lung nodules, cavitations, pleuritis and/or alveolar hemorrhages. Renal involvement affects 40–100% of patients as abnormalities in urine
sediment and renal failure. Other systemic manifestations may include arthralgia,
anorexia, weight loss, ocular involvement (episcleritis, uveitis, retinal thrombosis,
orbital pseudotumor…) myocarditis [11]. Recently, a new criteria set has been
approved and validated by the American College of Rheumatology (ACR) and the
European Alliance of Associations for Rheumatology (EULAR). The aim of the
classification criteria is to differentiate GPA from other types of small- or mediumvessel vasculitis (Table ) [13].
A limited form of GPA is defined by the presence of upper airways and/or pul-
monary involvement without alveolar hemorrhage. There is no renal involvement or
life-threatening conditions.
A diffuse or severe form of GPA is known by the presence of a severe renal
dysfunction and/or progressive alveolar hemorrhage and/or life-threatening organ
involvement.
Clinical criteria
Nasal involvement: bloody discharge ulcers, crusting, congestion, blockage, septal defect/
perforation
Cartilaginous involvement (inflammation, of ear or nose cartilage, hoarse voice or stridor,
endobronchial involvement or saddle nose deformity
Conductive or sensorineural hearing loss
Laboratory, imaging and biopsie criteria
Positive test for cytoplasmic antineutrophil cytoplasmic antibodies (c ANCA) or antiproteinase 3
(anti-PR3) antibodies
Pulmonary nodules, mass or cavitation on chest imaging
Granuloma, extravascular granulomatous inflammation or giant cells on biopsy
Pauci-immune glomerulonephritis on biopsy
Positive test for perinuclear antineutrophil cytoplasmic antibodies (pANCA) or
antimyeloperoxidase (anti-MPO) antibodies
Blood eosinophil count ≥1* 10
Tab le 1 .
2022 American college of rheumatology (ACR)/European alliance of associations for rheumatology [13].
9
/liter
+3
+2
+1
+5
+2
+2
+1
−1
−4
Pericarditis - Diagnosis and Management Challenges
73
.. Eosinophilic granulomatosis with polyangiitis
Eosinophilic granulomatosis with polyangiitis (EGPA) formerly known as Churg–
Strauss syndrome is a rare systemic small-vessel vasculitis associated with asthma
and eosinophilia. EGPA is the least common systemic vasculitis among AAV with an
annual incidence of 4.2 cases per million people and a prevalence of 10.7 per million
people [14]. It affects people aged between 40 and 60years with no gender predominance or ethnic predisposition [15, 16]. In 1990, ACR defined the classification
criteria for EGPA including asthma, eosinophilia >10%, neuropathy, non-fixed lung
infiltrates, paranasal sinus abnormalities and extravascular eosinophils on biopsy
(Table ) [17]. EGPA should be suspected in a patient with an adult-onset asthma and
multiple systemic manifestations (asymmetric neuropathy, purpura or skin ulcers,
cardiac, pulmonary and/or renal involvement …). Laboratory data show mainly
peripheral eosinophilia (>1500 cells/μL) correlated with the disease activity [18].
MPO-ANCA with perinuclear Immunofluorescence (pANCA) are noted in 50% [5].
Histologic findings confirm the leukocytoclastic vasculitis with eosinophilic granulomas in different biopsy sites (lung, kidney…).
.. Microscopic polyangiitis
MPA is a systemic necrotizing vasculitis with a pneumo-renal tropism. Capillaritis
is the cause of its main feature including alveolar hemorrhage and rapidly progressive glomerulonephritis. The annual incidence of MPA is about 5.8 cases per million
people [14]. MPA affects older patients compared to other AAV (between 50 and
60years) [19]. Some studies suggest that increased life expectancy may contribute to
the increased incidence of this disease [20]. Men are more frequently affected than
women [14]. Other clinical manifestations may include general signs (fever, weight
loss) in 70% of patients, skin lesions as vascular pupura, peripheral neuropathy,
liver dysfunction and gastrointestinal manifestations. MPO-ANCA are detected in
about 50% of cases, but its absence does not exclude its diagnosis [5]. Histological
data allow the differentiation of MAP from other AAV. This entity is characterized by
the absence of eosinophilic tissue infiltration found in GEPA and granulomas found
mainly in GPA but also in GEPA.
.. Five-factor score: a prognosis score of ANCA-vasculitis
The five-factor score (FFS) for AAV is used to evaluate prognosis at diagnosis of
the vasculitis. The following factors were significantly combined with higher fiveyear mortality: age>65years, cardiac involvement, renal insufficiency (creatinine
≥150μmol/L) and gastrointestinal symptoms. The presence of each was scored +1
1. Asthma
2. Eosinophilia >10%
3. Neuropathy (mono- or poly-neuropathy)
4. Non-fixed pulmonary infiltrates
5. Paranasal sinus abnormalities
6. Extravascular eosinophil infiltration on biopsy
At least four of the six ACR criteria are required.
Table 2.
ACR classification of EGPA [17].
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Age>65years
74
Cardiac insufficiency
Renal insufficiency (Creatinemia>150μmol/L)
Gastrointestinal involvement
Absence of ear, nose and throat manifestation for GPA and EGPA.
One point for each of these five items when present.
Table 3.
Revised 2011 Five-Factor score in AAV [21].
point. Whereas ear, nose and throat (ENT) involvement, affecting patients with GPA
and EGPA, were associated with a lower risk of death. Their absence was accorded +1
point (Tabl e ) [21].
. Treatment of granulomatosis with polyangiitis
The choice of treatments in GPA depends on several forms of the disease (limited
vs. diffuse), patient’s age, his overall physiological state and in particular his renal
function. At present, the choice of treatment according to the immunological profile
(ANCA-PR3, ANCA-MPO or ANCA-negative) remains a subject of controversy [22].
. Remission induction therapy
Regardless the clinical form of GPA, the treatment is based on a combination of
corticosteroids with immunosuppressant drug or rituximab. Corticosteroids are used
at a dose of 1mg/kg/day, preceded by methylprednisolone pulses (7.5 to 15mg/kg/
day) in severe or active cases. The choice of the immunosuppressant drug depends on
the clinical form and extent of the disease [22, 23].
. Non-severe or limited forms of granulomatosis with polyangiitis
Methotrexate, rituximab and cyclophosphamide are effective at inducing remission
the limited form of GPA. Although, methotrexate is currently recommended in this
patient group [24]. The weekly dose is 0.3mg/kg. According to the NORAM study, its
efficacy is comparable to that of cyclophosphamide with a lower risk of infection. Also,
mycophenolate mofetil (MMF) is effective as an induction therapy for the limited form
of GPA with satisfactory results. Rituximab may be used for patients with recurrent
relapses while receiving methotrexate or concerns regarding compliance [24].
. Severe or diffuse forms of granulomatosis with polyangiitis
Both rituximab and cyclophosphamide, in combination with glucocorticoids, have
been used for remission induction in GPA [24]. Corticosteroids with cyclophosphamide have always represented the gold standard in the treatment of diffuse forms
of GPA. Cyclophosphamide can be administrated per os (2mg/kg/day) or by intravenous pulses (15mg/kgevery 2 weeks for the first 3 pulses then every 3 weeks ) for
an initial duration of 3 to 6 months. According to the studies, they have comparable
results in terms of efficiency and average survival. However, due to the high cumulative dose of the oral route, this modality is associated with a high risk of infectious
Pericarditis - Diagnosis and Management Challenges
75
events [25, 26]. Rituximab or anti-CD20 is now preferred over cyclophosphamide
for many reasons. Its efficiency in inducing remission has been proven by numerous studies, especially for relapsed diffuse forms [22, 27, 28]. It is a better-tolerated
treatment and is considered less toxic than cyclophosphamide. It has lower risks of
malignancy and/or infertility. Also, the risk of infectious complications is almost the
same between these two drugs [29]. Rituximab has been approved for use in GPA as
a weekly infusion of 375mg/m2 for 4 consecutive weeks or as two 1-gram infusions
spaced two weeks apart. Currently, it is prescribed for relapsed patients, those of
childbearing age and/or those who have already received high cumulative doses of
cyclophosphamide. A duration of 3months may be required to achieve maximum
therapeutic benefit.
As in all AAVs and by extrapolation to their efficiency in Goodpasture’s syndrome,
plasma exchange is indicated in severe forms of GPA with alveolar hemorrhage and/or
glomerulonephritis. The MEPEX study showed their efficacy in patients with severe
renal impairment (creatinine level over 500 umol/l), but this action is not maintained
over the long term [30]. The benefit was most pronounced in patients with the highest
risk of end-stage renal disease [24]. Polyvalent immunoglobulins are recommended
for relapsing or severe disease. The total dose of infusions is 2g/kg over 2 or 5days.
. Remission maintenance therapy
To reduce its iatrogenicity, gradual tapering of corticosteroids is preferable after
inducing remission.
• Remission maintenance treatments for non-severe or limited forms of GPA are
based on the same immunosuppressant used in the induction phase (methotrexate,
MMF) [22]. Methotrexate should be taken for a long-term period (several years).
According to the NORAM study, stopping methotrexate at one year of progression
increases the risk of relapse of GPA [23]. For diffuse forms of GPA, methotrexate
and azathioprine represented the conventional remission maintenance drugs in
the last years. The WEGENT study concluded that they have comparable results
in terms of efficiency, safety and relapse frequency [31]. Rituximab is mentioned
in the latest European EULAR/ERA-EDTA guidelines as a remission maintenance
drug. Several prospective and retrospective studies have compared rituximab with
other molecules such as azathioprine. The results of these studies were in favor of a
greater reduction in the relapse rate of GPA by rituximab [22]. Therefore, rituximab
is now favored and highly recommended over methotrexate or azathioprine for
maintaining remission of severe GPA, but cost and other factors may limit rituximab use [24]. Upon remission of GPA, this biomedicine is started within 1month
of the last cyclophosphamide infusion or 4 to 6months after the start of rituximab
induction therapy. It is administered in 5 infusions of 500mg over 18months (at D1
and D15 then every 6months for 18months) (FDA-approved) [22].
. Treatment of eosinophilic granulomatosis with polyangiitis
. Conventional therapeutic regimen
Like other AAV, corticosteroids are the treatment’s cornerstone for GEPA.
Depending on the severity of the presentation, high-dose corticosteroids are oftenly
Current Treatment of ANCA Vasculitis
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initiated with pulses of methylprednisolone (15mg/kg). It is recommended for a
76
minimum period of 4weeks followed by a taper. This helps to control asthma, general
signs and hypereosinophilia [32]. Corticosteroids are prescribed alone or combined
with an immunosuppressant after evaluation of the clinical presentation by the FFS.
• If the FFS is equal to 0: These patients have no poor prognostic factors.
Corticosteroids are sufficient to achieve remission in more than 70% of cases
[32]. Cyclophosphamide is used in case of relapse or resistance to corticosteroids
[33]. Survival rates in this group are important even in case of relapse.
• If the FFS is equal to or more than 1: Intravenous pulse cyclophosphamide should
be combined. Treatment strategy recommends 6 pulses in less than 4months
(15mg/kg every two weeks for three doses and then every three weeks for three
doses). For remission maintenance, azathioprine at a dose of 2mg/kg/day or
methotrexate at a dose of 0.3mg/Kg/week will be used for 12 to 18months
depending on the evolution [34].
. Therapeutic alternatives
There have been very few randomized controlled trials conducted to date in EGPA.
Rituximab is not yet validated as an alternative to cyclophosphamide in GEPA. Due to
the rarity of this disease compared to other AAV, a small number of therapeutic trials
have been reported in the literature with conflicting results. Some studies confirm the
efficiency of this biomedicine especially in case of relapse [35–38] and particularly in
patients with a positive vasculitis/anti-MPO profile [39]. Nevertheless, in addition to
infectious complications, rituximab has been incriminated in the occurrence of severe
bronchospasm secondary to a hypersensitivity reaction [39].
Recently, interleukin-5 inhibitors have been introduced into the GEPA therapeutic
regimen. Mepolizumab is a humanized monoclonal antibody against interleukin-5. It
has been approved for use in severe eosinophilic asthma. In refractory forms of GEPA,
it was effective in remission induction and maintenance due to its immunosuppressive
properties [40, 41]. A recent international randomized, controlled and double-blind
study compared the effect of mepolizumab versus placebo in refractory GEPA treated
with corticosteroids combined or not with immunosuppressive treatment. Long-term
remission of GEPA was noted in the group using mepolizumab [42].
Anti-IgE drugs such as omalizumab have been used during severe allergic asthma.
For GEPA, the results of the use of this biomedicine are variable and contradictory. As
previously described, omalizumab has been incriminated as an unmasking factor for
underlying vasculitis [43]. Other studies suggest its efficacy during GEPA especially
for pulmonary relapses but also as a cortisone-sparing agent [44, 45]. In conclusion,
further data are needed before omalizumab can be recommended or contraindicated
in the treatment of GEPA [36].
. Treatment of microscopic polyangiitis
Management of MPA is based on remission induction therapy and remission
maintenance therapy. For non-renal forms with an FFS equal to zero, corticosteroids
are used alone as a first-line treatment to induce remission. An immunosuppressant
will be associated in case of non-response, relapse or dependence on corticosteroids
Pericarditis - Diagnosis and Management Challenges
77
but also in case of extension to a systemic form with involvement of other organs (cardiac, renal, CNS …). However, high-dose corticosteroids associated with rituximab or
cyclophosphamide are recommended for severe forms of MPA with a life-threatening
outcome [22]. Azathioprine and methotrexate have been validated as remission
maintenance treatments [31]. By extrapolation of their efficacy in good pasture’s
syndrome, plasma exchange is indicated in fulminant forms of MPA with severe renal
involvement and/or alveolar hemorrhage. Currently, rituximab is also recommended
for remission induction in case of refractory disease [28].
. Associated treatments in ANCA-associated vasculitis
Management of AAV includes other therapeutic measures such as local and/
or surgical treatment of ENT manifestations in GPA and EGPA (nasal irrigations,
Type of
vasculitis
GPA/MPA Remission
EG PA Remission
GPA: granulomatosis with polyangiitis, MPA: microscopic polyangiitis, EGPA: eosinophilic granulomatosis with
polyangiitis, GCs: glucocorticoids MTX: methotrexate, AZA: azathioprine, MMF: mycophenolate mofetil, CYC:
cyclophosphamide, MEP: mepolizumab, ENT: ear nose throat.
Phase of
treatment
induction
therapy
Remission
maintenance
therapy
induction
therapy
Remission
maintenance
therapy
Form of
vasculitis
Active nonsevere/limited
form of GPA
Active severe
form of GPA/
MPA
Non-severe/
limited form
of GPA
severe form of
GPA/MPA
Active nonsevere form of
EG PA
Active severe
form of EGPA
Non-severe
limited form
of EGPA
severe form of
EG PA
Recommendation/
statement
High dose of GCs+MTX
(over CYC, RTX, AZA or
MMF)
High dose of GCs+RTX
(over CYC)
GCs +
MTX, AZA or MMF
(continue the same
medication)
Patients whose disease
has entered remission
after treatment with CYC
or RTX :
GCs+RTX (over MTX
or AZA
GCs alone or with
MEP (over MTX, AZA or
MMF)
High dose of GCs+either
CYC or RTX (over MEP)
CGs _
Patients whose disease has
entered remission after
treatment with CYC:
GCs+MTX, AZA or
MMF
(over RTX or MEP)
Level of
evidence
Very low to
moderate
_
Very low to
moderate
Very low to
low
Ver y l ow
Ver y l ow
Associated
treatment
-Cotrimoxazole
-Local or surgical
treatment of ENT
manifestations
-Kinesitherapy
and symptomatic
treatments for
neuropathic
manifestations
Table 4.
Recommendations/statements for the management of ANCA vasculitis [24].
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nebulizations, polyposis resection …), kinesitherapy and symptomatic treatments
78
for neuropathic symptoms and hemodialysis in end-stage renal disease. In addition,
complications related to the long-term use of corticosteroids should be managed
(hypertension, diabetes …) [28].
Cotrimoxazole (trimethoprim/sulfamethoxazole) is highly recommended in AAV
and should be discussed in case of lymphopenia. Especially in GPA, it prevents from
pneumocystis and has a role in remission maintenance of this vasculitis (Table ).
. Conclusion
Significant advancements in pathogenic knowledge helped to improve the man-
agement and the prognosis of patients suffering from AAV. This group of rare systemic vasculitis has now earlier remissions and lower relapse rates but needs urgent
and aggressive treatment based on corticosteroids and immunosuppressant agents
most of the time. Nowadays, rituximab has gained popularity because of his efficiency and less toxic properties. It is now preferred in severe cases of GPA and MPA.
It was even more potent than cyclophosphamide in relapsing forms of the diseases.
Our understanding of the pathogenesis continues to expand, and targeting specific
pathogenic pathways is needed to improve the outcome.
Pericarditis - Diagnosis and Management Challenges
79
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